Why I
Joined GGCP

Honestly, GGCP is not where I thought I would be at this point in my life. I also think that this is the very best place for me to be right now. I have always wanted a career in veterinary health and medicine. After majoring in Animal Science at California Polytechnic State University, I worked in the poultry industry as a production and health supervisor. I found I loved the health aspects of my position and wanted to broaden my experiences in that area. So, I obtained a position as a postgraduate researcher at UC Davis. The studies I was involved with included using nonhuman primates as models for allergic airway diseases, including asthma. It was at this time that I found a desire to be involved in utilizing animal models for studies of human diseases. GGCP is an ideal bridge between animal and human health. It gives me the opportunity to understand the relationship between human and animal disease processes and treatments. My work now focuses on the host's immune response to inhaled environmental toxicants. I am using an animal model to study the effects of toxicants to which humans are exposed on a daily basis. After completing my PhD, I plan to work in the industry of drug development. Through preclinical trials, I can utilize the information I obtained and developed through GGCP to understand the relationship between human and animal health.

Exposure to air pollutants is a significant factor in exacerbating lung diseases, including asthma and chronic obstructive pulmonary disease. An important component of air pollution, especially in urban areas, is diesel exhaust. Many of the components of diesel exhaust, especially nitropolyaromatic hydrocarbons, are recognized as pulmonary cytotoxicants and contributors to the mutagenic activity of respirable airborne particles. 1-nitronaphthalene is a nitropolyaromatic hydrocarbon that has been widely detected in ambient urban air and is created by the atmospheric gas phase reaction of nitric oxides (N₂O₅) and naphthalene. 1-nitronapthalene lung injury includes activation of reactive metabolites followed by an inflammatory response that expands the extent of acute injury.

Acute pulmonary injury is often associated with an inflammatory reaction. Neutrophils are the major component of the inflammatory response to many pulmonary toxicants and there is conflicting evidence regarding the role of the neutrophil. Activated neutrophils release powerful inflammatory mediators, reactive oxygen intermediates, and proteolytic enzymes that damage both cellular and extracellular tissue components. On the other hand, neutrophils help to clear injured and necrotic cells, enhancing new cell growth.

To determine the role of the neutrophil in cytotoxicity, inflammatory responses, and epithelial repair from exposure to 1-nitronaphthalene, we are blocking neutrophils in a rat model with an anti-neutrophil antibody prior to exposure to 1-nitronaphthalene. We are then evaluating cytotoxicity and epithelial repair between neutrophil-depleted and neutrophil-sufficient rats. The ultimate goal of this project is to understand the effect of neutrophils in response to 1-nitronaphthalene in hopes of improving therapeutics for lung disease.

Figure 1. Airway epithelium of an untreated adult rat.

Figure 2. Airway epithelium of a neutrophil-depleted rat treated with 1-nitronaphthalene.

Figure 3. Airway epithelium of a neutrophil-sufficient rat treated with 1-nitronaphthalene.